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Background: Gallbladder hypomotility is a key pathogenic factor in cholelithiasis. Non-invasive interventions to enhance gallbladder contractility remain limited. Ultrasound therapy has shown promise in various muscular disorders, but its effects on gallbladder function are unexplored.
Methods: This study employed low-intensity pulsed ultrasound (LIPUS) at a 3 MHz frequency and 0.8 W/cm intensity with a 20% duty cycle to irradiate the gallbladder region of fasting guinea pigs. Gallbladder contractile function was evaluated through multiple complementary approaches: in vivo assessment via two-dimensional/three-dimensional ultrasound imaging to monitor volumetric changes; quantitative functional evaluation using nuclear medicine scintigraphy (Tc-HIDA); and ex vivo experiments including isolated gallbladder muscle strip tension measurements, histopathological analysis, α-smooth muscle actin (α-SMA) immunohistochemistry, and intracellular calcium fluorescence imaging.
Results: Ultrasound significantly enhanced gallbladder emptying, evidenced by the volume reduction and increased ejection fraction. Scintigraphy confirmed accelerated bile transport in treated animals. Ex vivo analyses demonstrated augmented contractile force, amplitude, and frequency in ultrasound-treated smooth muscle. Histological examination revealed smooth muscle hypertrophy, α-SMA upregulation, and elevated intracellular calcium levels. Extended ultrasound exposure produced sustained functional improvements without tissue damage.
Conclusions: Ultrasound effectively enhances gallbladder contractile function through mechanisms involving smooth muscle structural modification and calcium signaling modulation. These findings establish the experimental foundation for ultrasound as a promising non-invasive therapeutic approach to improve gallbladder motility and potentially prevent gallstone formation.
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http://dx.doi.org/10.3390/bioengineering12070716 | DOI Listing |
Front Med (Lausanne)
August 2025
Royal College of Surgeons in Ireland - Bahrain, Al-Muharraq, Bahrain.
Introduction: Ischemic heart disease (IHD) remains a major global health burden, highlighting the urgent need for early, non-invasive diagnostic biomarkers. MicroRNAs (miRNAs), small non-coding RNA molecules that regulate gene expression, have emerged as promising candidates due to their stability in circulation and involvement in cardiovascular processes. This systematic review aimed to evaluate the potential of specific miRNAs as early diagnostic biomarkers in IHD.
View Article and Find Full Text PDFJ Interferon Cytokine Res
September 2025
Department of Nephrology, The First Affiliated Hospital of Guangxi University of Chinese Medicine, Guangxi, China.
Hirudin, a polypeptide extracted from medicinal leeches, has demonstrated potential in treating renal fibrosis. This study aimed to explore the underlying mechanisms by which Hirudin alleviates renal fibrosis. Renal fibrosis models were established using unilateral ureteral obstruction (UUO) surgery in rats and transforming growth factor-β (TGF-β)-induced HK-2 cells, followed by treatment with different concentrations of Hirudin.
View Article and Find Full Text PDFCurr Drug Metab
September 2025
First School of Clinical Medicine, Yunnan University of Chinese Medicine, Kunming 650500, China.
Background: Tetrandrine (TET) demonstrates therapeutic potential for hypoxic pulmonary hypertension (HPH); however, its precise pharmacological mechanisms remain unclear. In this study, we aimed to investigate the effects of TET on pulmonary vascular remodeling (PVR) in HPH and elucidate the molecular pathways through which TET ameliorates HPH.
Methods: We established a rat model of HPH and evaluated the therapeutic effects of TET by measuring hemodynamic parameters, assessing right ventricular hypertrophy, and analyzing pathological changes in lung tissue.
Biomed Pharmacother
September 2025
Department of Anatomy and Regenerative Biology, Graduate School of Medicine, Osaka Metropolitan University, Osaka, Japan.
Liver fibrosis, which eventually leads to cirrhosis, is characterized by excessive accumulation of type I collagen (COL1A), mainly derived from activated hepatic stellate cells (HSCs). Currently, there is no clinical treatments that can directly address this condition. The objectives of this study were to identify a compound that can suppress HSC activation and elucidate the molecular mechanism underlying its action.
View Article and Find Full Text PDFLung
September 2025
The Wellcome-Wolfson Institute for Experimental Medicine, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, 97 Lisburn Road, Belfast, Belfast BT9 7BL, UK.
Introduction: Rhinovirus (RV) is the leading cause of exacerbations of lung disease. A sensory neuronal model, derived from human dental pulp stem cells and differentiated into peripheral neuronal equivalents (PNEs), was used to examine RV's effects on airway sensory nerves. We investigated whether RV can directly infect and alter PNEs or whether it exerts effects indirectly via the release of mediators from infected epithelial cells.
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